With the recently available advances in chemical carcinogenesis in laboratory animals and availability of techniques to measure gastric mucosal permeability and gastric function, we plan to study a prototype of a dietary carcinogen with respect to those conditions which seemingly predispose man to gastric carcinoma. We aim to: (1) measure the absorption of this agent from canine gastric pouches under "normal" conditions for such a model; (2) measure changes in the rate of absorption of the carcinogen during the course of months so that the gastritis which it produces can itself be evaluated in relation to barrier function and increased carcinogen absorption; (3) measure absorption of the carcinogen when the barrier is acutely disrupted by bile or aspirin-acid solutions; (4) produce chronic inflammatory change, and persistent barrier dysfunction in animal models by means of repeated bile-acid instillations, and after this is accomplished and verified to measure absorption of the carcinogen; (5) quantitate changes in mucosal barrier function resulting from the gastritis and intestinal metaplasia produced by the carcinogen, and to relate these anatomical changes to the physiochemical ones; and (6) measure absorption rates, and (test effectiveness of) carcinogens which are not ordinarily well absorbed by the stomach and yielding only poor rates of cancer production in the glandular stomach in laboratory animals. This is of special interest to us in order to test a hypothesis: certain dietary carcinogens may not ordinarily be absorbed into the gastric mucosa, and are not effective there because of the normal function of mucosal barrier.